Holstein (n = 19) and Jersey (n = 18) cows were used to study effects of two feeding systems on fatty acid composition of milk. Confinement cows were fed a total mixed ration with corn silage and alfalfa silage and pastured cows grazed a crabgrass (90%) and clover (10%) pasture and were allowed 5.5 kg of grain per head daily. Two milk samples were collected from each cow at morning and afternoon milkings 1 d each week for four consecutive weeks in June and July 1998. One set of milk samples was analyzed to determine fatty acid composition, and the second set was used for crude protein and total fat analyses. Data were analyzed by the general linear models procedure of SAS, using a split-plot model with breed, treatment, and breed x treatment as main effects and time of sampling and week as subplot effects along with appropriate interactions. Milk from pastured cows was higher than milk from confinement cows for the cis-9, trans-11 octadecadienoic acid isomer of conjugated linoleic acid (CLA). Also, milk from Holsteins was higher than milk from Jerseys for C16:1, C18:1, and CLA and lower than Jerseys for C6:0, C8:0, C10:0, C12:0, and C14:0. Several treatment x week interactions existed, but main effects were still important; for example, proportions of CLA in milk of grazed cows were relatively constant across weeks (0.66, 0.64, 0.64, and 0.69% +/- 0.02%, respectively), but the CLA in milk of confinement cows increased in wk 4 (0.35, 0.31, 0.31, and 0.48% +/- 0.02% for wk 1 to 4, respectively). There are potentially important differences in fatty acid composition of milk from cows consuming a warm season pasture species compared with milk from cows consuming a total mixed ration, as well as differences between Holstein and Jersey breeds.

A B S T R A C T Total and unbound testosterone and A4-androstenedione have been determined in 104 cord blood samples. The same sexual steroids and pituitary gonadotropins have been measured in 46 normal male infants aged 27-348 days and 34 normal female infants aged 19-332 days.In cord blood of female neonates mean total and unbound testosterone was 29.6±7.5 and 0.89±0.4 ng/100 ml, respectively (mean±l SD); A4-androstenedione was 93±38 ng/100 ml. In male neonates mean plasma total and unbound testosterone was 38.9±10.8 and 1.12±0.4 ng/100 ml; A'-androstenedione was 85±27 ng/100 ml.In female infants testosterone concentrations remained constant during the lst yr of life with a mean concentration of 7±3 ng/100 ml. Mean unbound testosterone and A'-androstenedione concentrations were 0.05±0.03 and 16.7±8.3 ng/100 ml, respectively. Mean plasma levels of follicle-stimulating hormone and luteinizing hormone were 8.7±3.3 and 12.9±7.7 mU/ml.In male infants mean plasma total testosterone concentration increased to 208±68 ng/100 ml from birth to 1-3 mo of age, decreasing thereafter to 95±53 ng/100 ml at 3-5 mo, 23.2±18 ng/100 ml at 5-7 mo, and reached prepubertal levels (6.6±4.6 ng/100 ml) at 7-12 mo.Mean unbound testosterone concentration plateaued from birth to 1-3 mo of age (1.3±0.2 ng/100 ml) decreasing to prepubertal values very rapidly. Mean A4-androstene-

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Congenital adrenal hyperplasia (CAH) is caused by disorders of the P450c21B gene, which, with the P45Oc21A pseudogene, lies in the HLA locus on chromosome 6. The near identity of nucleotide sequences and endonuclease cleavage sites in these A and B loci makes genetic analysis of this disease difficult. We used a genomic DNA probe that detects the P45Oc21 genes (A pseudogene, 3.2 kb; B gene, 3.7 kb in Taq leles thus can easily be classified with this new probing strategy, eliminating many ambiguities resulting from probing with cDNA.

Plasma free dehydroepiandrosterone (DHA), androstenedione (delta), testosterone (T), dihydrotestosterone (DHT), estrone (E1), and estradiol (E2) were measured by radioimmunoassay in 55 boys and 54 girls 3.5 to 16.3 years of age. Plasma DHA increased significantly between 6 and 8 years of age in girls and between 8 and 10 years of age in boys. A further significant increase was noted between 10 and 12 years of age in both sexes. Delta rose significantly between 8 and 10 years of age in girls and between 10 and 12 years in boys. In contrast, no significant increase in T, DHT, or E1, was noted prior to 12 years of age in both sexes. However, E2 showed a significant increase between 10 and 12 years of age in girls. This early rise in the course of pubertal development of the two sex steroids predominantly of adrenal origin, DHA and delta, and its occurence 1 to 2 years earlier in girls than in boys, as does puberty itself, suggest a possible role for these steroids in the mechanisms involved in triggering the hypothalamic-pituitary-gonadal axis at puberty.

A patient with familial male pseudohermaphroditism was considered to be a normal female up to the time of puberty. At puberty, she had normal breast development but there was simultaneous enlargement of the clitoris and the body hair developed with a male distribution. The internal genitalia were male in type. Under basal conditions, the plasma concentration of testosterone (T) was low for a male subject but plasma levels of dehydroepiandrosterone (DHA) and dehydroepiandrosterone sulfate (DHAS) were 2-3 times higher than those of normal men. The plasma level of androstenedione (A) was 10 times normal. Following gonadectomy, the pattern of plasma androgens was similar to that of a normal woman. Prior to operation, the basal urinary excretion of estrone, estradiol and estriol was much increased above that of a normal man but it became normal after gonadectomy. Eighteen months after gonadectomy, both before and after adrenal stimulation, the plasma androgens showed the pattern and concentrations expected in the normal adult female. The same could be said of the peripheral in terconversion between T & A. The data strongly suggest that the patient had an incomplete 17-ketosteroid reductase defect and that this defect was limited to the testes. (J Clin Endocr 32: 604, 1971)

A sensitive and reliable radioimmunoassay combined with celite column chromatography for specific determination of plasma testosterone (T) is described. The percentage binding was measured by equilibrium dialysis.In 28 normal newborns, total T concentration is significantly higher in male (68.1 ± 59.5) than in female newborn infants (12.0 ± 6.2) while binding of T increases rapidly after birth. Although there is no sex difference in TeBg capacity, levels of unbound T in the first two weeks of life are still significantly higher in male than in female infants.There was no sex difference in 62 normal prepubertal children studied, the total T concentration being 6.62 ± 2A6 and 6.58 ± 2.48 ng/100 ml in boys and girls, respectively; the binding of T and unbound T levels were identical in both.In 17 patients with Turner syndrome, total T concentration (13.6 ± 3.1 ng/100 ml) was significantly higher than in prepubertal children and increased (21.S ± 2 ng/100 ml) under moderate estrogen therapy while the percentage of T bound to protein did not change (96.65% ± 0.29 and 96.81% rfc 1.4 respectively). However unbound T levels remained 1/4 to 1/2 that of normal adult females.In 13 patients with primary hypogonadism, total T concentration was similar to that of Turner patients (13.12 ± 5.4 ng/100 ml) so as were the percentage of T bound to proteins and unbound T levels. The physiological implications of free and bound testosterone concentrations in newborns, prepuberal and hypogonadal children are discussed. ( / Clin Endocrinol Metab 36: 1132, 1973

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